Ellen Kamhi, PhD, RN and Eugene Zampieron, ND, AHG examine Osteoporosis, a disease of the skeletal system.

by Ellen Kamhi, PhD, RN and Eugene Zampieron, ND, AHG

Osteoporosis is a disease of the skeletal system, which is characterized by deterioration of bone tissue, along with a decrease in bone mass. It can strike anyone at any age, although it is most prevalent in Caucasian and Asian, small boned woman over 50 years old. Osteoporosis is recognized as a major public health issue. Over 10 million Americans are afflicted, with 34 million more who may already be exhibiting signs of low bone mass, which increases the risk of developing osteoporosis.1 It can effect any bone in the body, although the most common sites are the wrist, spine and hips. It is credited with more than 1.5 million fractures per year, causing a huge amount of personal suffering and loss of quality of life.2 This disease also has a high cost to society, with an estimated hospital and nursing home expenditure of 18 billion dollars in 2002 due to osteoporotic hip fractures alone.

The term, ‘osteoporosis’, clearly describes the condition of the inside of the bones in this disease, where large porous areas develop, weakening bone structure. Bone mass decreases due to an increase in the activity level of osteoclasts, which cause bone reabsorption, as compared to osteoblasts, responsible for bone building. After reaching a ‘fracture threshold’, bone that was normally able to withstand a minor stress, such as a fall or blow, becomes subject to break or fracture more easily. Although osteoporosis is often diagnosed in the senior years, building healthy bone during the first 3 decades of life, by providing sufficient bone building nutrients, along with weight bearing exercise, may be the best protection against this disease.3 

There are several risk factors that increase the chance for an individual to develop osteoporosis: family history, female (six to eight times more likely than male) especially post-menopausal, due to decreased estrogen levels, advancing age, caucasian, low calcium intake, smoking, alcohol consumption, soft drink consumption,4 and a sedentary lifestyle. Since many of these, and other contributing factors, are self regulated, pharmacists can have a direct impact on this health issue by diligently educating customers. Risk of osteoporosis is also directly linked to the use of many prescription and OTC drugs: corticosteroids/steroids, thyroid hormones, anticonvulsants, aluminum containing antacids, loop diuretics, and gonadotropin-releasing hormones, among others. Wherever possible, pharmacists can instruct customers about natural therapies that may be equally effective for specific health conditions, but present a substantially lower risk for interfering with bone density.

Drug therapies for osteoporosis include bisphosphonates, such as alendronate and risedronate. A once per month tablet, ibandronate sodium, claims the advantage of greater convenience, but still has a host of possible adverse effects such as esophageal irritation, heartburn, and ulcers. In addition, it is not recommended that women with hypocalcemia take these drugs, while many women with osteoporosis have low calcium levels! Hormone replacement therapy was previously touted as a treatment, and may, in fact be quite useful for decreasing bone loss. However, this benefit decreases if hormone therapy is discontinued. In addition, many women refuse hormone therapy due to other known and perceived adverse effects.5 Although these pharmaceutical agents can be effective, there is an increased interest in non-pharmacological prevention and treatment of osteoporosis.6 Pharmacists can be proactive on this front by supporting the improvement of nutritional status through diet and nutritional supplementation, along with suggestion for an increase in exercise training.

There are several natural interventions that promote increased bone health. These include regular exercise, and nutritional supplements including calcium, magnesium, phosphorous, boron, strontium and herbal isolates including ipriflavones.7 


Exercise has an important impact on bone health. Several studies have increased awareness on how exercise can most constructively be used to prevent the development of osteoporosis. Starting to exercise at a young age is best to achieve long-term positive effects. High impact activities maximize the osteogenic response. Mechanical loading is site specific- therefore rotate exercise sites, focusing on each one for a limited time period, while increasing the number of exercise sessions. This helps to offsetdesensitization of mechano-transduction pathways. Continuing to exercise throughout life helps to reduce bone loss and risk of falls.8 


Calcium is the most abundant mineral in the human body. It is well-recognized for its importance in the development of bones and teeth, and has many other functions as well. Calcium acts as a ‘pump’ regulation mechanism that escorts nutrients and waste products in and out of cells through their membranes. It is also involved in nerve transmissions and muscle contractions. The best food sources of calcium include whole grains, beans, almonds and other nuts, and dark green leafy vegetables, such as kale. Milk and dairy products contain a lot of calcium, but the absorption of calcium from dairy by the body can be slow due to the high amount of protein in these foods. It is interesting to note that individuals who avoid dairy due to lactose intolerance do not experience a corresponding increase in osteoporosis.9 Calcium supplements have been shown to be effective at slowing bone loss in both peri-menopausal and post menopausal women.10 The ability of calcium supplements to “maintain good bone health and reduce the high risk of osteoporosis later in life.” is one of the few health label claims allowed by the United States FDA. In addition, calcium delivers beneficial support for premenstrual syndrome complaints (ie. bloating, weight gain, breast tenderness, headaches, muscle cramps and mood swings.)11 

To maintain bone health, 1000- 1500mg/day of calcium (including food sources and supplements) is recommended (varies with age, weight, sex, etc.) by the National Academy of Sciences. 12 It is often difficult to get this amount through diet alone; supplementation is often called for. . This can be confusing, due to the many forms of calcium on the market, the differences in dosage levels, absorption rates, delivery forms (ie tablets, vs. liquids), cost, etc.  Several studies have shown that calcium citrate is absorbed better than tricalcium phosphate, calcium lactate and calcium carbonate, (the kind of calcium in antacid tablets).13 Calcium citrate does not tend to cause gastric distress, and has a pleasant taste. One study surmised that calcium formate is better absorbed than either calcium citrate or calcium carbonate.14 Since calcium is so intimately involved in an array of metabolic reactions, it is not surprising that there is a long list of possible interactions with pharmaceutical drugs. Examples follow. Calcium decreases the absorption of bisphosphonates15, levothyroxine16, tetracycline and quinolone antibiotics17 while Thiazide can reduce calcium excretion, leading to hypercalcemia, metabolic alkalosis and renal failure.18 The pharmacist can assist customers to choose a calcium supplement that best meets their needs.


Magnesium is the second most common mineral in the body (after calcium). Magnesium is important for many metabolic processes, including building bone, formation of ATP, and promoting calcium absorption. Dietary sources of magnesium include nuts, whole grains, dark green vegetables, fish, meat and legumes. Magnesium is often deficient in the Standard American Diet, due to eating a diet low in this nutrient, and soil depletion due to commercial farming practices. Low levels of blood magnesium correlates with low bone density,19 and several studies have supported the use of oral magnesium supplementation  to increase bone density.20 Even a moderate magnesium deficiency can cause bone loss.21 Magnesium deficiency may impair the production of parathyroid hormone and 1,25-dihydroxyvitamin D, which negatively effects bone mineralization.22 Supplementing with 250-350 mg a day of magnesium is usually recommended. Magnesium glycinate or gluconate are preferable to magnesium oxide, and are less likely to cause loose stools. Adverse effects of magnesium usually occur at higher dosages, and are often associated with intravenous magnesium. Drug interactions include neuromuscular weakness and possible paralysis when combined with aminoglycoside antibiotics, decreased absorption of biphosphates, tetracycline antibiotics and calcium channel blockers(take at different times). Conversely, many drugs cause hypomagnesemia , including aldesleukin, aminoglycosides and amphotericin-B(common).23 Magnesium supplementation helps to balance a number of health issues in addition to osteoporosis, such as insomnia, headaches, chronic constipation, restless leg syndrome, anxiety and irritability, and is often the first supplement we recommend in our clinical practice.

Vitamin D

Vitamin D is produced by the body through the activity of the sun; hence the name, the ‘sunshine vitamin’. It is essential for the formation of bone tissue. Vitamin D deficiency is common among people in northern latitudes, the elderly, and others who don’t regularly get enough sun exposure. Vitamin D-3, most closely matches natural vitamin D, formed by the body. There is a plethora of recent research on the positive health benefits of Vitamin D supplementation, along with the widespread occurrence of Vitamin D deficiency. It is prudent to access all patients for Vitamin D status, and recommend supplementation of from 400 IU to 2000 IU’s and above, depending on individual status.


Boron is ubiquitous throughout the human body with the highest concentrations found in the bones and dental enamel. Although there is currently no RDA, boron appears to be indispensable for healthy bone function, possibly via effects on reducing the excretion and absorption of calcium, magnesium and phosphorus.24 and by affecting signal transmissions across cell membranes. 25 Boron may be involved in the synthesis of steroidal vitamins and hormones, such as  Vitamin D, 17 beta-estradiol and testosterone26 and  inhibits a range of microsomal enzymes which catabolize  these steroids, thus delivering a net up-regulatory effect, which could explain its bone building properties.27   Boron clusters or carboranes have a high binding affinity for steroidal receptors28 and are being formulated into medications such as specific enzyme inhibitors.29 Boron may be beneficial in the treatment of osteoporosis, especially in the case of vitamin D, magnesium, and potassium deficiency.30 

Fruits, vegetables, soybeans and nuts can be rich sources of boron, but the level depends on the soil in which it is grown. A safe daily intake is estimated to be between 1 and 10 mg. Sodium borate is the most common form of supplement. Toxic effects appear at intakes of about 100 mg. A fatal dose in adults is 15 to 20 g and in children 3 to 6 g. Repeated intakes of small amounts can cause accumulative toxicity.


The mineral strontium is a powerful agent in the treatment and prevention of osteoporosis. Strontium is a naturally occurring mineral present in water and food. Trace amounts of strontium are found in the human skeleton, where it is absorbed at the matrix crystal surface of bones. The Spinal Osteoporosis Therapeutic Intervention study is a double-blind, randomized, placebo-controlled trial, which compared two groups of postmenopausal women who already had a diagnosis of osteoporosis. One group was given two grams daily of non-radioactive strontium ranelate , while another group received a  placebo. The strontium group illustrated a significant reduction (41%) in the relative risk of experiencing a new vertebral fracture.31 Other promising studies showed reduced risks for nonvertebral fractures, including hip fractures.32 In addition to reducing the risk of fracture, strontium ranelate increased bone mineral density throughout the study, peaking at 3 years, with augmented scores of  8.2% in the femoral neck and 9.8%  in the total hip. Japanese pharmaceutical researchers have trade named the strontium salt PROTELOS and are in phase two drug trials. In the US, strontium is available as a dietary supplement in the form of strontium citrate. Is important to ensure calcium and vitamin D intakes are adequate when supplementing with strontium. This is underscored by earlier research on animals suggesting that increasing the intake of strontium via diet may demineralize bone when calcium is deficient.33 In rats with chronic kidney failure, strontium has been shown to cause osteomalacia, a condition in which bone is softened due to lack of mineral content. For this reason, people on kidney dialysis should not use strontium supplements.34


Research supports the positive effects of soy isoflavones for reducing the risk of developing osteoporosis.35 Diets high in soy may decrease bone re-absorption in postmenopausal women.36 Although ipriflavone, a semi synthetic flavone comparable to genistein and diadzein found in soy foods, was ineffective in restoring bone density in rats, it modulated IGF-I(insulin growth factor I),37 which is linked to bone mineral density and increased bone remodeling through several mechanisms.38 IGF-I is currently being measured by holistic health practitioners as one of the parameters to assess overall aging. Ipriflavone yielded positive results on increasing bone in human trials at doses of 200 mg per day,39 and seems particularly beneficial when combined with calcium.40 The authors postulate that increased soy consumption is a reasonable and prudent measure due to scientific validation of its positive effects, combined with a low incidence of adverse reactions.  Soy can cause allergic reactions in some individuals, and may inhibit thyroid hormone synthesis.41

Health care practitioners can be instrumental in educating their patients to the fact that, with intelligent dietary and lifestyle choices, osteoporosis is largely preventable for most people.

Additional articles and resources on this topic:


1 National Osteoporosis Foundation website: http://www.nof.org/osteoporosis/diseasefacts.htm

2 Sawka AM, Thabane L, Papaioannou A, et. al.Health-related quality of life measurements in elderly Canadians with osteoporosis compared to other chronic medical conditions: a population-based study from the Canadian Multicentre Osteoporosis Study (CaMos). Osteoporos Int. 2005 Aug 18

3 Davies JH, Evans BA, Gregory JW. Bone mass acquisition in healthy children. Arch Dis Child. 2005 Apr;90(4):373-8.

4 Wyshak G, Frisch RE. Carbonated beverages, dietary calcium, the dietary calcium/phosphorus ratio, and bone fractures in girls and boys. J Adolescent Health 1994;15:210–5. and Mazariegos-Ramos E, Guerrero-Romero F, Rodríquez-Morán F, et al. Consumption of soft drinks with phosphoric acid as a risk factor for the development of hypocalcemia in children: a case-control study. J Pediatr 1995;126:940–2.

5 Schonberg MA, Davis RB, Wee CC. After the Women’s Health Initiative: decision making and trust of women taking hormone therapy. Womens Health Issues. 2005 Jul-Aug;15(4):187-95)(Selby P.Postmenopausal osteoporosis. Curr Osteoporos Rep. 2004 Sep;2(3):101-6.

6 Ishikawa-Takata K, Ohta T. Nonpharmacological prevention and treatment for osteoporosis. Clin Calcium. 2005 Sep;15(9):1463-6.

7 Borer KT.Physical activity in the prevention and amelioration of osteoporosis in women : interaction of mechanical, hormonal and dietary factors. Sports Med. 2005;35(9):779-830

8 Warden SJ, Fuchs RK, Turner CH. Steps for targeting exercise towards the skeleton to increase bone strength. Eura Medicophys. 2004 Sep;40(3):223-32.

9 Enattah N, Pekkarinen T, Valimaki MJ, et. al., Genetically defined adult-type hypolactasia and self-reported lactose intolerance as risk factors of osteoporosis in Finnish postmenopausal women. Eur J Clin Nutr. 2005Oct;59(10):1105-11

10 Di Daniele N, Carbonelli MG, Candeloro N,, et. al. Effect of supplementation of calcium and vitamin D on bone mineral density and bone mineral content in peri- and post-menopause women; a double-blind, randomized, controlled trial. Pharmacol Res. 2004 Dec;50(6):637-41

11 Bertone-Johnson ER, Hankinson SE, Bendich A, et. al. Calcium and vitamin D intake and risk of incident premenstrual syndrome. Arch Intern Med. 2005 Jun 13;165(11):1246-52.

12 Standing Committee on the Scientific Evaluation of Dietary Reference Intakes, Food and Nutrition Board, Institute of Medicine. Dietary reference intakes for calcium, phosphorus, magnesium, vitamin D and fluoride. Washington DC: National Academy Press, 1997, 108–17

13 Heaney RP, Rafferty K, Dowell MS , et. al.Calcium fortification systems differ in bioavailability. J Am Diet Assoc. 2005 May;105(5):807-9

14 Hanzlik RP, Fowler SC, Fisher DH.. Relative bioavailability of calcium from calcium formate, calcium citrate, and calcium carbonate. J Pharmacol Exp Ther. 2005 Jun;313(3):1217-22.

15 Peters ML, Leonard M, Licata AA. Role of alendronate and risedronate in preventing and treating osteoporosis. Cleve Clin J Med 2001;68:945-51.

16 Schneyer CR. Calcium carbonate and reduction of levothyroxine efficacy. JAMA 1998;279:750.

17 Pletz MW, Petzold P, Allen A, et al. Effect of calcium carbonate on bioavailability of orally administered gemifloxacin. Antimicrob Agents Chemother 2003;47:2158-60.

18 Friedman PA, Bushinsky DA. Diuretic effects on calcium metabolism. Semin Nephrol 1999;19:551-6.

19 Saito N, Tabata N, Saito S, et. al. Bone mineral density, serum albumin and serum magnesium. J Am Coll Nutr. 2004 Dec;23(6):701S-3S.

20 Katsumata SI, Matsuzaki H, Uehara M, et. al. Effect of dietary magnesium supplementation on bone loss in rats fed a high phosphorus diet. Magnes Res. 2005 Jun;18(2):91-6. and Stendig-Lindberg G, Tepper R, Leichter I. Trabecular bone density in a two year controlled trial of peroral magnesium in osteoporsis. Magnes Res 1993;6:155-63.

21 Rude RK, Gruber HE, Norton HJ, e.t, al. Dietary magnesium reduction to 25% of nutrient requirement disrupts bone and mineral metabolism in the rat. Bone. 2005 Aug;37(2):211-9.

22 Rude RK, Gruber HE. Magnesium deficiency and osteoporosis: animal and human observations. J Nutr Biochem. 2004 Dec;15(12):710-6.

23 Sabra R, Branch RA. Amphotericin B nephrotoxicity. Drug Saf 1990;5:94-108.

24 Nielsen FH, Hunt CD, Mullen LM et al. Effect of dietary boron on mineral, estrogen, and testosterone metabolism in postmenopausal women, FASEB J 1987;1:394-397

25 Barr RD, Barton SA, Schull WJ. Boron levels in man: preliminary evidence of genetic regulation and some implications for human biology. Med Hypotheses 1996;46:286-289

26 Nielsen FH, Hunt CD, Mullen LM et al. Effect of dietary boron on mineral, estrogen, and testosterone metabolism in postmenopausal women, FASEB J 1987;1:394-397

27 Miljkovic N, McCarty MF. Up-regulatory impact of boron on vitamin D function — does it reflect inhibition of 24-hydroxylase? Med Hypotheses. 2004;63(6):1054-6

28 Endo Y, Yamamoto K, Kagechika H. Utility of boron clusters for drug design. Relation between estrogen receptor binding affinity and hydrophobicity of phenols bearing various types of carboranyl groups. Bioorg Med Chem Lett. 2003 Nov 17;13(22):4089-92

29 Cigler P, Kozisek M, Rezacova P, et. al.From nonpeptide toward noncarbon protease inhibitors: Metallacarboranes as specific and potent inhibitors of HIV protease. Proc Natl Acad Sci U S A. 2005 Oct 14

30 Schaafsma A, de Vries PJ, Saris WH.Delay of natural bone loss by higher intakes of specific minerals and vitamins. Crit Rev Food Sci Nutr. 2001 May;41(4):225-49

31 Reginister JY, Sarlet, N, Lejeune, E, et. al. Strontium ranelate: a new treatment for postmenopausal osteoporosis with a dual mode of action. Curr Osteoporos Rep. 2005 Mar;3(1):30-4.

32 Reginister JY, Seeman E, DeVernejoul, MCet al. Strontium ranelate reduces the risk of nonvertebral fractures in postmenopausal women with osteoporosis: Treatment of Peripheral Osteoporosis (TROPOS) study J Clin Endocrinol Metab. 2005 May;90(5):2816-22. Epub 2005 Feb 22.

33 Grynpas MD, Marie PJ. Effects of strontium on bone quality and quantity in rats. Bone 1990;11:313-19

34 Schrooten, I, Cabrera W, Goodman WG, et al. Strontium causes osteomalacia in chronic renal failure in rats. Kidney Int 1998;54:448-56

35 Uenishi K. Recommended soy and soy products intake to prevent bone fracture and osteoporosis. Clin Calcium. 2005 Aug;15(8):1393-8.

36 Harkness LS, Fiedler K, Sehgal AR, et al. Decreased bone resorption with soy isoflavone supplementation in postmenopausal women. J Womens Health (Larchmt). 2004 Nov;13(9):1000-7

37 Deyhim F, Smith BJ, Soung do Y et al. Ipriflavone modulates IGF-I but is unable to restore bone in rats. Phytother Res. 2005 Feb;19(2):116-20

38 Niu T, Rosen CJ. The insulin-like growth factor-I gene and osteoporosis: A critical appraisal. Gene. 2005 Sep 21

39 Passeri M, Biondi M, Costi D et al. Effect of Ipriflavone on bone mass in elderly osteoporotic women. Bone Miner 1992: 19(suppl 1):S57-62

40 Gennari C, Agnusdei D, Crepaldi G, et al. Effect of ipriflavone–a synthetic derivative of natural isoflavones–on bone mass loss in the early years after menopause. Menopause. 1998 Spring;5(1):9-15

41 Persky VW, Turyk ME, Wang L, et al. Effect of soy protein  on endogenous hormones in postmenopausal women. J Clin Nutr 2002;75:145-53.)

Ellen Kamhi, The Natural Nurse®,  and Eugene ZampieronDr. Z Naturally, are the authors of The Natural Medicine Chest and Arthritis, The Alternative Medicine Guide. Dr. Zampieron is a Professor of Botanical Medicine at Bridgeport College of Naturopathic Medicine and Ellen Kamhi is a Professional Herbalist with Nature’s Answer in Hauppauge, NY.